Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA169026 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The transcriptional repressor Zbtb20 is essential for specification of hippocampal CA1 pyramidal neurons. Moreover, ectopic expression of Zbtb20 is sufficient to transform subicular and retrosplenial areas of D6/Zbtb20S mice to CA1. We used microarrays to identify genes that are repressed by Zbtb20 in developing CA1 pyramidal neurons in the CA1-transformed cortex of D6/Zbtb20S mice.
2014-04-11 | GSE38837 | GEO
Project description:The transcriptional repressor Zbtb20 is essential for specification of hippocampal CA1 pyramidal neurons. Moreover, ectopic expression of Zbtb20 is sufficient to transform subicular and retrosplenial areas of D6/Zbtb20S mice to CA1. We used microarrays to identify genes that are repressed by Zbtb20 in developing CA1 pyramidal neurons in the CA1-transformed cortex of D6/Zbtb20S mice. For RNA extraction and hybridization on Affymetrix microarrays, we isolated the CA1-transformed subiculum and retrosplenial cortex from postnatal day 1 D6/Zbtb20S mice, as well as corresponding areas from their wildtype littermates. Total RNA was extracted using the RNeasy Lipid Tissue Mini Kit (Qiagen). Each RNA sample represents a pool of RNA obtained from dissected tissues of seven animals.
2014-04-11 | E-GEOD-38837 | biostudies-arrayexpress
Project description:RNA-Seq from CA1 pyramidal neurons
| PRJNA557516 | ENA
Project description:RNA-Seq from CA1 pyramidal neurons purified by FACS from 4-week-old mice.
2020-01-07 | GSE135147 | GEO
Project description:Spatial gene expression gradients underlie prominent heterogeneity of CA1 pyramidal neurons
| PRJNA279837 | ENA
Project description:Neurodegenerative brain disorders become more common in the aged. Most of these disorders are associated with or caused by selective death of certain neuronal subpopulations. The mechanisms underlying the differential vulnerability of certain neuronal populations are still largely unexplored and few neuroprotective treatments are available to date. Elucidation of these mechanisms may lead to a greater understanding of the pathogenesis and treatment of neurodegenerative diseases. Moreover, preconditioning by a short seizure confers neuroprotection following a subsequent prolonged seizure. Our goal is to identify pathways that confer vulnerability and resistance to neurotoxic conditions by comparing the basal and preconditioned gene expression profiles of three differentially vulnerable hippocampal neuron populations. Hippocampal CA1 and CA3 pyramidal neurons are highly susceptible to seizures and ischemia, whereas dentate gyrus granule cells are relatively resistant. A brief preconditioning seizure confers protection to the pyramidal cells. We will first determine gene expression profiles of untreated rat CA1 and CA3 pyramidal cells, and dentate granule cells, using laser capture microscopy to obtain region-specific neuronal mRNA. We will then determine the effect of a brief preconditioning seizure, which is neuroprotective in CA1 and CA3, on these expression profiles. We hypothesize that common molecular mechanisms exist in neurons that determine their susceptibility to seizure-induced injury. Intrinsic differences in gene expression exist between hippocampal glutamatergic CA1 and CA3 pyramidal neurons, on the one hand, and dentate granule cells on the other, which contribute to the greater susceptibility of pyramidal neurons to degeneration in experimental stroke and epilepsy. We specifically hypothesize that differences in basal energy metabolism genes may confer differential susceptibility to neurodegeneration produced by seizures and ischemia. Anesthetized animals will be sacrificed by decapitation, and frozen 10 micron sections will be lightly stained with cresyl violet to identify cell layers in the hippocampus. Approximately 1000 neurons from each of the three cell layers will be isolated by LCM. Poly-A RNA will be amplified using a modified Eberwine protocol. The quality of our aRNA will be evaluated by quantitative RT-PCR of GluR6 and KA2 mRNA levels before we send the samples to the Center for labeling and hybridization to Affymetrix rat 230A arrays. We will provide a one-round amplification cDNA product to the center for labeling and hybridization. This protocol is identical to a previously approved study by Jim Greene in our laboratory.
2007-09-18 | E-GEOD-1994 | biostudies-arrayexpress
Project description:FMRP cTag CLIP from mouse CA1 pyramidal neurons
| PRJNA525639 | ENA
Project description:Complete global brain ischemia (CGBI) and reperfusion occur following resuscitation from cardiac arrest. Different brain neurons are selectively vulnerable to CGBI: pyramidal neurons of hippocampal CA3 survive 10 min CGBI but those of CA1 die at 3 days following 10 min CGBI. CA3 neurons are expected to have more robust stress responses and repair responses than CA1 neurons. We used microarrays to compared total and polysome-bound mRNAs in CA1 and CA3 at 8 hr reperfusion after 10 min CGBI in Long Evans male rats to ascertain differences in total vs polysome-bound gene expression.
2016-06-02 | GSE82146 | GEO
Project description:Triggering receptor expressed on myeloid cells 2 (Trem2) is a myeloid cell-specific gene expressed in microglia, whose variants are associated with multiple neurodegenerative diseases. TREM2 receptor modulates phagocytosis, cytokine production and metabolism, enabling appropriate surveillance of the brain by microglia and ensuring their proper response to damage signals. Here, we demonstrate that TREM2 plays a key role in controlling the bioenergetic profile of pyramidal neurons during development. In the absence of Trem2, developing neurons in hippocampal CA1 -but not in CA3- subfield display compromised energetic metabolism and defective basal, maximal and ATP-dependent respiration, accompanied by reduced mitochondrial mass and abnormal organelle ultrastructure. This is paralleled by a significant transcriptional rearrangement of hippocampal pyramidal neurons at birth, with a pervasive alteration of metabolic, oxidative phosphorylation and mitochondrial signatures. The developmental trajectories of the excitatory lineages indicate that lack of Trem2 causes a delay in the maturation of CA1 neurons, paired with specific alterations in the mitochondrial TOM complex which persist in the mature hippocampus. In addition, the mitochondrial defects and faulty neuronal differentiation are maintained also after neuron isolation from the brain context, suggesting that the lack of TREM2-mediated communication between microglia and neurons at early developmental windows is sufficient to derange the forthcoming maturation of neuronal metabolism. Our results unveil a novel role of TREM2 in controlling neuronal development by regulating the metabolic fitness of neurons in a region-specific manner.
2024-01-15 | GSE249036 | GEO
Project description:AMPA receptors are involved not only in neuronal plasticity but also in excitotoxicity, mediated largely by the influx of Ca2+ (Choi et al., 1988). Their implication has been highlighted in animal models of ischemia and epilepsy. Studies of ischemic rodent models featured that prior to cell death, hippocampal CA1 pyramidal cells exhibit an increased AMPA receptor-mediated Ca2+ influx and decreased GluR2 and GluR3 mRNA and protein levels (Gorter et al., 1997; Heuerteaux et al., 1995). A total of 15 RNA samples were analyzed. Cultured murine primary cortical neurons were treated with 300uM AMPA over a time-course of 5h, 15h and 24h (n=3) in addition to the vehicle control (n=6).
2013-12-31 | E-GEOD-22993 | biostudies-arrayexpress